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Biomedical subjects

V E Nahmod

Publications and source records attributed to V E Nahmod.

At least 73 records · Page 4Linked to original sources
PubMed1978

Angiotensin regulates release and synthesis of serotonin in brain.

Angiotensin II released serotonin from neuron terminals and accelerated synthesis of the serotonin. This increase in synthesis depended on the activation of tryptophan hydroxylase. A biphasic effect was observed: at high doses the stimulatory effect depended on conversion of angiotensin II to angiotensin III. At low doses an inhibitory effect was found, possible dependent on an angiotensin II metabolite. These actions represent a subtle regulation of the open-loop serotonin system.

Angiotensin II↗
PubMed1971

Angiotensin and renin in rat and dog brain.

An enzyme with the characteristics of classical renin was isolated from brain extracts of nephrectomized dogs. This enzyme is thermolabile, nondialyzable, and forms a vasoconstrictive material when incubated with renin plasma substrate at pH 7. A short lasting pressor activity was also found in brain extracts of dogs and rats. This activity was due to a substance identified by chemical and pharmacological tests as angiotensin. Countercurrent distribution of brain extracts of rats showed that 38% of the pressor activity corresponded to angiotensin II and the remainder to angiotensin I. A remarkable correlation was found between angiotensin and norepinphrine concentrations in different portions of the encephalon of the dog.

Angiotensin II↗
PubMedDate not supplied

Muscarinic M1 receptors in the lateral septal area mediate cardiovascular responses to cholinergic agonists and bradykinin: supersensitivity induced by chronic treatment with atropine.

The infusion of pilocarpine, acetylcholine, bradykinin and the selective M1 muscarinic agonist McNeil-A-343 into the lateral septal area produced a dose-dependent increase of arterial blood pressure and heart rate. The M1 muscarinic agonist carbamylcholine that causes a rise in arterial blood pressure when injected into the anterior lateral ventricles did not produce any cardiovascular effects when infused into the lateral septal area. Chronic treatment with atropine induced supersensitivity to the muscarinic agonists and a significant increase in the number of muscarinic receptors. In this study bradykinin failed to produce any significant change in cardiovascular activity. Pirenzepine, a M1 muscarinic blocking agent, inhibited completely the effect of both muscarinic agonists and bradykinin on cardiovascular activity. In fact, in vitro studies shows that the displacement of the binding of [3H]QNB by pirenzepine is compatible with the presence of the M1 subtype of muscarinic receptor in the lateral septal area, where it may play a major role on cardiovascular regulation.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMedDate not supplied

Glucocorticoids inhibit the autoregulatory induction of interleukin-1 in monocytes after endotoxin stimulation.

Interleukin-1 (IL-1) is an important mediator in the mechanisms underlying the immune and inflammatory responses. It has pleiotropic effects in host defense and, when present in high concentrations, participates in the development of pathological processes. IL-1 is the most potent cytokine in the activation of the hypothalamic-pituitary-adrenal axis during infection and therefore leads to a glucocorticoid increase. Glucocorticoids in a feedback loop inhibit the production of IL-1 induced by endotoxin. IL-1 also induces its own synthesis. In this report, we examine the role of glucocorticoids in the regulation of IL-1 autoregulatory induction in human monocytes at the level of IL-1 protein production and mRNA accumulation. Using recombinant IL-1 receptor antagonist we established that endogenously produced IL-1 affects induction of IL-1beta protein by lipopolysaccharide (LPS) at the level of mRNA expression. The inhibition of LPS-stimulated IL-1beta production and mRNA expression by glucocorticoids (dexamethasone and cortisol) reaches the same level with glucocorticoids alone or in combination with rIL-1ra. IL-1beta mRNA induced by exogenously added IL-1beta was also inhibited by glucocorticoids. These results indicate that glucocorticoids inhibit the autoregulatory loop of IL-1 in LPS-stimulated monocytes and constitute a mechanism for controlling IL-1 feedback stimulation.

Cells, Cultured↗